Hypertrophic scars and keloids affect an estimated 10% of the population. While a variety of therapeutic modalities have been attempted, the majority of medical and surgical specialties treating these problems agree that these are notoriously difficult to treat. Currently over 50% of our population is aged forty-five years or older. With more minimally invasive procedures becoming available, more patients seek elective aesthetic surgical procedures. With cutaneous laser exfoliation procedures on the rise, there has also been an increased incidence of facial hypertrophic scars. While more deeply pigmented skin is susceptible, any person may develop a persistent hypertrophic scar or keloid following a traumatic injury or surgical intervention. These types of scars are more common in areas which demonstrate slow wound healing response, such as the anterior chest, and in movement-dependent areas, such as the scapula, elbow, and knee. A hypertrophic scar is usually raised and erythematous, but remains within the confines of the original traumatic wound. In contrast, a keloid is a more nodular lesion which extends beyond the margins of the initial wound.
For centuries physicians have studied the processes of wound healing. Wound healing is complicated, but generally can be divided into three overlapping phases. There is an inflammation phase, a granulation tissue formation phase, and a matrix formation or remodeling phase. Studies have revealed that these phases overlap. Considerable study has gone into the modification of these phases, with the hope of gaining some control over the overall wound healing mechanism. For decades, scars were an accepted phenomenon. Patients were told that there was little that could be done, and had to come to accept the appearance of their scars. Many patients have stimulated the interest of researchers to attempt to modify the healing process, since many patients do not readily accept that nothing can be done to improve the appearance of what they may perceive as somewhat disfiguring scars.
A general understanding of the phases of healing is important to an understanding of scar modification parameters. The first phase of wound healing is the inflammatory phase. During this stage, there is a release of mediators which sets the stage for the formation of granulation tissue. This inflammatory phase can be divided into an early and a late period. The early period starts immediately with the wounding of the skin. The initial trauma causes bleeding into the wound space. Subsequent to normal hematosis, the exposure of blood to fibrillar collagen and tissue factor starts the intrinsic and extrinsic clotting cascades. The aggravation of platelets also triggers the coagulation cascade and contributes to hemostasis. The habradic kinen is released through activated factor 12. This stimulates the classic compliment cascade to begin. This subsequently causes the release of anaphylatoxins and subsequent vascular permeability-ability with chemotaxis of white blood cells.
During the early portion of the inflammatory phase neutrophils and monocytes appear in the wound space. First, neutrophils appear approximately six hours after the insult. Monocytes arrive somewhat later. The main function of the neutrophils in early wound healing is to debride the wound of particulate and bacterial contamination. The disappearance of neutrophils from the wound space signals the end of the early inflammatory phase of wound healing. This is usually seen within one to two days.
In contrast to the neutrophil, monocytes persist in the wound space and play a more significant role. The persistence of macrophages marks the late segment of the inflammatory phase. Macrophages continue with the debridement of the wound by phagocytizing bacteria and debris.
The second phase of wound healing, known as the granulation phase, is characterized by granulation tissue formation. Within the granulation phase of wound healing, the processes of angiogenesis, re-epithelialization and collagen synthesis occur. The main cells involved in this phase include macrophages, the fibroblasts, epithelial cells and endothelial cells. These cells work together under the direction of growth factors and other mediators. Extracellular matrix is also formed during this phase. This matrix which is comprised of fibronectin and collagen is a critical component to the wound healing. Extracellular matrix is composed primarily of proteoglycans, fibronectin, and collagen. The aforementioned cells act in unison to facilitate the processes of re-epithelialization and neovascularization.
Remodeling is the third and final phase of wound healing. It is during this phase that the extracellular matrix is reorganized and collagen converted from type 3 collagen to type 1 collagen. It is during this phase that wound contraction also occurs. Wound contraction involves a complex interaction between fibroblasts, fibronectin, and collagen. Several models of remodeling suggest that fibroblasts are recruited into the wound via the chemotactic properties of various growth factors. Once a critical mass of fibroblasts exists within the wound, fibronectin and type 1 collagen are then produced. Fibroblasts align themselves within the fibronectin-collagen extracellular lattice. Wound contraction can then occur through this tightly arranged network of fibroblast, fibronectin, and collagen.
As the remodeling phase continues, fibronectin disappears from the wound and is replaced by collagen. Collagen continues to occupy more of the wound space and the wound breaking strength begins to increase. As type 1 collagen surpasses type 3 collagen, the breaking strength once again shows an increase. Typically a final scar ultimately obtains a breaking strength 70% that of uninjured skin.
A variety of treatments for hypertrophic scars and keloids have been advocated in the past. These include intralesional steroids, cryosurgery, radiotherapy, pressure therapy, silicone gel sheeting, laser therapy, and excisional surgery. Recurrences remain common, and patient satisfaction is variable. Many patients are also dissatisfied with the increased erythema in the wound.